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首页> 外文期刊>Infection and immunity >MyD88- and TRIF-Independent Induction of Type I Interferon Drives Naive B Cell Accumulation but Not Loss of Lymph Node Architecture in Lyme Disease
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MyD88- and TRIF-Independent Induction of Type I Interferon Drives Naive B Cell Accumulation but Not Loss of Lymph Node Architecture in Lyme Disease

机译：I型干扰素的MyD88和TRIF依赖性诱导可促进幼稚B细胞积累，但不会使莱姆病中的淋巴结结构丧失。

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Rapidly after infection, live Borrelia burgdorferi, the causative agent of Lyme disease, is found within lymph nodes, causing rapid and strong tissue enlargement, a loss of demarcation between B cell follicles and T cell zones, and an unusually large accumulation of B cells. We sought to explore the mechanisms underlying these changes, as lymph tissue disruption could be detrimental for the development of robust Borrelia-specific immunity. A time course study demonstrated that the loss of the normal lymph node structure was a distinct process that preceded the strong increases in B cells at the site. The selective increases in B cell frequencies were due not to proliferation but rather to cytokine-mediated repositioning of B cells to the lymph nodes, as shown with various gene-targeted and bone marrow irradiation chimeras. These studies demonstrated that B. burgdorferi infection induced type I interferon receptor (IFNR) signaling in lymph nodes in a MyD88- and TRIF-independent manner and that type I IFNR indirect signaling was required for the excessive increases of naive B cells at those sites. It did not, however, drive the observed histopathological changes, which occurred independently also from major shifts in the lymphocyte-homing chemokines, CXCL12, CXCL13, and CCL19/21, as shown by quantitative reverse transcription-PCR (qRT-PCR), flow cytometry, and transwell migration experiments. Thus, B. burgdorferi infection drives the production of type I IFN in lymph nodes and in so doing strongly alters the cellular composition of the lymph nodes, with potential detrimental effects for the development of robust Borrelia-specific immunity.
机译：感染后迅速在淋巴结内发现了活的伯氏疏螺旋体（莱姆病的病原体），引起快速而牢固的组织增大，B细胞滤泡和T细胞区之间的分界丧失以及B细胞异常大的积累。我们试图探索这些变化的潜在机制，因为淋巴组织破坏可能对强大的疏螺旋体特异免疫力的发展有害。一项时程研究表明，正常淋巴结结构的丧失是一个明显的过程，该过程是该部位B细胞大量增加之前的过程。 B细胞频率的选择性增加不是由于增殖，而是由于细胞因子介导的B细胞重新定位到淋巴结，如各种针对基因的和骨髓照射嵌合体所示。这些研究表明，B。burgdorferi感染以MyD88和TRIF独立的方式在淋巴结中诱导I型干扰素受体（IFNR）信号传导，而这些部位的幼稚B细胞过度增加则需要I型IFNR间接信号传导。然而，它并没有驱动观察到的组织病理学变化，该变化也独立于淋巴细胞归巢趋化因子CXCL12，CXCL13和CCL19 / 21的主要变化，如定量逆转录PCR（qRT-PCR）所示细胞计数和Transwell迁移实验。因此，B。burgdorferi感染驱动淋巴结中I型IFN的产生，并因此强烈改变了淋巴结的细胞组成，具有发展强大的疏螺旋体特异免疫力的潜在有害作用。

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